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AIP1 Suppresses Transplant Arteriosclerosis Through Inhibition of Vascular Smooth Muscle Cell Inflammatory Response to IFNγ
Author(s) -
Qin Lingfeng,
Min Wang,
Xin Shijie
Publication year - 2019
Publication title -
the anatomical record
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.678
H-Index - 62
eISSN - 1932-8494
pISSN - 1932-8486
DOI - 10.1002/ar.24040
Subject(s) - arteriosclerosis , vascular smooth muscle , inflammatory response , medicine , inflammation , immunology , smooth muscle , cardiology
IFNγ‐induced vascular smooth muscle cells (VSMCs) inflammatory response plays a key role in transplant arteriosclerosis (TA). However, the mechanisms regulating this process remains poorly defined. Here, we show that ASK1‐interacting protein 1 (AIP1) deletion markedly augments the expression of IFNγ‐induced chemokines in mouse aortic allografts. Subsequently, donor arterial grafts from AIP1 deficient mice exhibited an accelerated development of TA. Furthermore, AIP1 knockdown significantly increased IFNγ signaling activation in cultured VSMCs and thus enhances chemokines production in response to IFNγ. Together, we conclude that AIP1 functions as an inhibitor of VSMCs inflammation by regulating IFNγ signaling and therefore suppresses TA progression. Our findings suggest that AIP1 might be a potential therapeutic target for chronic transplant rejection. Anat Rec, 302:1587–1593, 2019. © 2018 American Association for Anatomy